Implantable neurostimulation systems have proven therapeutic in a wide variety of diseases and disorders. For example, Spinal Cord Stimulation (SCS) techniques, which directly stimulate the spinal cord tissue of the patient, have long been accepted as a therapeutic modality for the treatment of chronic pain syndromes, and the application of spinal cord stimulation has begun to expand to additional applications, such as angina pectoralis and incontinence.
An implantable SCS system typically includes one or more electrode carrying stimulation leads, which are implanted at a stimulation site in proximity to the spinal cord tissue of the patient, and a neurostimulator implanted remotely from the stimulation site, but coupled either directly to the stimulation lead(s) or indirectly to the stimulation lead(s) via a lead extension. The neurostimulation system may further comprise a handheld patient programmer to remotely instruct the neurostimulator to generate electrical stimulation pulses in accordance with selected stimulation parameters. The handheld programmer may, itself, be programmed by a technician attending the patient, for example, by using a Clinician's Programmer (CP), which typically includes a general purpose computer, such as a laptop, with a programming software package installed thereon.
Thus, programmed electrical pulses can be delivered from the neurostimulator to the stimulation lead(s) to stimulate or activate a volume of the spinal cord tissue. In particular, electrical stimulation energy conveyed to the electrodes creates an electrical field, which when strong enough, depolarizes (or “stimulates”) the neural fibers within the spinal cord beyond a threshold level, thereby inducing the firing of action potentials (APs) that propagate along the neural fibers to provide the desired efficacious therapy to the patient.
The combination of electrodes used to deliver electrical pulses to the targeted tissue constitutes an electrode combination, with the electrodes capable of being selectively programmed to act as anodes (positive), cathodes (negative), or left off (zero). In other words, an electrode combination represents the polarity being positive, negative, or zero. Other parameters that may be controlled or varied include electrical pulse parameters, which may define the pulse amplitude, pulse width, pulse rate, pulse shape, and burst rate. Each electrode combination, along with the electrical pulse parameters, can be referred to as a “stimulation parameter set.”
Stimulation energy may be delivered to the electrodes during and after the lead placement process in order to verify that the electrodes are stimulating the target neural elements and to formulate the most effective stimulation regimen (i.e., the best stimulation parameter set or sets). The stimulation regimen will typically be one that provides stimulation energy to all of the target tissue that must be stimulated in order to provide the therapeutic benefit, yet minimizes the volume of non-target tissue that is stimulated.
While the electrical stimulation of neural fibers has generally been successful in providing a therapeutic benefit to the patient, there are instances where the target tissue is not directly adjacent to an electrode and, because the electrical field strength decreases exponentially with distance from the electrodes, a relatively strong electrical field must be created to generate APs in the target neural fibers. The electrical field may, however, also result in the generation of APs in non-target neural fibers between the electrode and the target neural fibers. The generation of APs in the non-target neural fibers may, in turn, lead to undesirable outcomes (e.g., discomfort or involuntary movements) for the patient. Because the target neural tissue (i.e., the tissue associated with the therapeutic effects) and non-target neural tissue (i.e., the tissue associated with undesirable side effects) are often juxtaposed, therapeutically stimulating neural tissue while preventing side effects may be difficult to achieve. In the context of SCS, there may be a few ways of eliminating, or at least minimizing, the stimulation of non-target neural tissue.
For example, to provide pain relief without inducing involuntary motor movements or otherwise causing discomfort, the neural fibers in the dorsal column (DC neural fibers), which primarily include sensory neural fibers, may be preferentially stimulated over neural fibers in the dorsal roots (DR neural fibers), which include both innocuous sensory neural fibers and sensory fibers linked directly to motor reflexes.
It is believed that the antidromic activation (i.e., the APs propagate in a direction opposite to their normal direction, which in the case of the spinal cord DC neural fibers, propagate in the caudal direction) of the large diameter DC neural fibers provides the actual pain relief to the patient by reducing/blocking transmission of smaller diameter pain fibers via interneuronal interaction in the dorsal horn of the spinal cord, while the orthodromic activation (i.e., the APs propagate in their normal direction, which in the case of the spinal cord, propagate in the rostral direction) of the large diameter DC neural fibers generate APs that arrive at the thalamus and are relayed to the sensory cortex, thereby creating a typically innocuous side-effect in the form of a sensation known as paresthesia, which can be characterized as an tingling sensation.
Thus, it is believed that the large diameter DC neural fibers are the major targets for SCS for overlaying the patient's painful regions with paresthesia. It can then be appreciated that the clinical goal of pain relief can often be achieved by placing the electrodes of the stimulation lead(s) as near as possible to the innervating DC neural fibers associated with the dermatomic area of pain, and if necessary, “tuning” the electrical stimulation by adjusting one or more stimulation parameters. In some cases, this is relatively simple due to the relatively close proximity of the active stimulating electrodes to the innervating DC neural fibers, as well as the size and/or orientation of the stimulating electrodes relative to these DC neural fibers.
However, in many clinical situations, the targeted DC neural fibers are difficult to stimulate for the inverse of the above reasons. In these cases, stimulation tuning can be difficult and can require great skill, insight, and luck. Typically, such tuning entails confining the stimulating electrical field to a region of neural tissue that has a high likelihood of achieving concordant paresthesia using primarily electrode combination adjustments, and then attempting improve neural selectivity using electrical pulse parameter adjustments. This method, however, can be self-limiting. If the targeted neural fibers are close to, outnumbered by, and/or harder to stimulate than the non-targeted neural fibers, it may be that the non-targeted neural fibers are stimulated to a greater degree than the targeted neural fibers, or even to a degree that the patient finds intolerable. As a result, even if the DR neural fibers are not stimulated, over-stimulation of the DC neural fibers may occur, thereby resulting in a discomfort sensation that is thought to originate from the orthodromic propagation of the APs to the thalamus of the patient.
An example of this phenomenon is commonly experienced clinically. In particular, if the patient seeks concordant paresthesia for lower back pain, a stimulation lead may be placed along the spinal cord and the stimulation parameters selected to activate the DC neural fibers that innervate the L1-L2 dermatomes coincident with the lower back body region. However, the L1-L2 dermatomes are also coincident with the anterior legs. Because the DC neural fibers that innervate the lower back region are likely to be less prevalent and perhaps deeper in the spinal column than the DC neural fibers that innervate the anterior leg regions, it is likely that a great many anterior leg-innervating neural fibers will reside in the superficial layers of the dorsal column and will be activated at lower stimulation energy than the lower back-innervating neural fibers.
Thus, it is often the case that the patient will perceive leg paresthesia as the first paresthesia perception and, as the magnitude of the stimulation energy is increased in an attempt to achieve lower back paresthesia, the leg paresthesia grows more intense, while the lower back paresthesia is not yet achieved. At some point, the leg paresthesia becomes too intense to be tolerated, such that the magnitude of the stimulation energy may not be further increased. If the DC neural fibers that innervate the low back region are only partially stimulated, or not stimulated at all, at the maximum tolerated stimulation energy, then the therapy will be highly compromised (if existent).
There, thus, remains a need to minimize or eliminate any adverse effect that may otherwise result from the inadvertent stimulation of non-targeted neural tissue.